Femoral anteversion related to side differences in hip rotation: Passive rotation in 1, 140 children aged 8-9 years

We assessed whether the range of passive hip motion is reliable for predicting abnormal femoral ante-version. We measured the passive medial and lateral rotation in extension in both hips of 1, 140 children between 8 and 9 years of age. The children were divided into 3 groups: group 1: difference between lateral and medial rotation less than 10° group 2: medial rotation more than 10° greater than the lateral; group 3: lateral rotation more than 10° greater than the medial. Group 1 comprised 90% of the children, whereas 8% belonged to group 2 and 2% to group 3.

The angle of femoral neck anteversion was measured in 57 children from the first group, in 67 from the second and in 24 children from the third group, using biplane radiography. The mean anteversion angles in the 3 groups were 24°, 36° and 14°, respectively. To predict an abnormally high anteversion angle (above mean +2SD), the difference between medial and lateral rotation must be 45° or more, whereas an abnormally low anteversion angle (lower than mean -2SD) could be predicted when the lateral rotation was at least 50° higher than the medial rotation.     

HnRNP CBP35-CBP67 interaction during stress response and ageing

Previous studies have demonstrated the existence of nuclear carbohydrate binding proteins in a variety of mammalian cells with molecular masses of 35 000, 67 000, and 70 000 (CBP35, CBP67, and CBP70), which are associated with nuclear ribonucleoprotein (RNP) complexes. CBP35 consists of two domains, an aminoterminal portion that is homologous to certain regions of proteins of the heterogeneous nuclear RNP complex, and a carboxyl-terminal portion homologous to β-galactoside-specific lectins. CBP35 it has been proposed, like the glucose-specific lectin, CBP67, to guide RNP complexes through the nuclear pore. Here we show that the exposure of mature rats to stress induces an increase in nuclear CBP35 bound to CBP67 and retained on immobilized glucose. Nuclear extracts from the livers of old rats displayed no detectable stress response. This CBP35·CBP67 association detected in rat liver is considered with respect to the CBP35·CBP70 association recently observed in HL60 cell nuclear extracts.     

Increased central adiposity is associated with pro-inflammatory immunoglobulin G N-glycans

Background

Increased body fat may be associated with an increased risk of developing an underlying pro-inflammatory state, thus leading to greater risk of developing certain chronic conditions. Immunoglobulin G has the ability to exert both anti- and pro-inflammatory effects, and the N-glycosylation of the fragment crystallisable portion is involved in mediating this process. Body mass index, a rudimentary yet gold standard indication for body fat, has been shown to be associated with agalactosylated immunoglobulin G N-glycans.

Inhibition of cellular responses to insulin in a rat liver cell line. A role for PKC in insulin resistance

The initial response of liver cells to insulin is mediated through exocytosis of Cl⁻ channel-containing vesicles and a subsequent opening of plasma membrane Cl⁻ channels. Intracellular accumulation of fatty acids leads to profound defects in metabolism, and is closely associated with insulin resistance. It is not known whether the activity of Cl⁻ channels is altered in insulin resistance and by which mechanisms. We studied the effects of fatty acid accumulation on Cl⁻ channel opening in a model liver cell line. Overnight treatment with amiodarone increased the fat content by ∼2-fold, and the rates of gluconeogenesis by ∼5-fold. The ability of insulin to suppress gluconeogenesis was markedly reduced indicating that amiodarone treatment induces insulin resistance. Western blot analysis showed that these cells express the same number of insulin receptors as control cells. However, insulin failed to activate exocytosis and Cl⁻ channel opening. These inhibitory effects were mimicked in control cells by exposures to arachidonic acid (15 μ m ). Further studies demonstrated that fatty acids stimulate the PKC activity, and inhibition of PKC partially restored exocytosis and Cl⁻ channel opening in insulin-resistant cells. Accordingly, activation of PKC with PMA in control cells potently inhibited the insulin responses. These results suggest that stimulation of PKC activity in insulin resistance contributes to the inhibition of cellular responses to insulin in liver cells.     

Myoid hamartomas of the breast: report of 3 cases and review of the literature

Hamartomas were first described by Albrecht in 1904, who defined them as tumor-like malformations in which there was abnormal blending of the normal components of an organ. The myoid hamartoma is a rare benign lesion of the breast and has an uncertain origin, possibly in the walls of the blood vessels, muscularis mammillae of the areolae, and mainly in myoepithelium. We report 3 cases of myoid hamartomas of the breast, with the clinical, radiologic, and histopathological findings, and review the literature. The 3 lesions showed normal breast ducts and lobules, entrapped by a muscular stroma and some foci of mature adipose tissue. The muscular origin of part of the stroma was confirmed by strong reactiveness with smooth-muscle actin.     

Minimal intervention dentistry for managing dental caries – a review

This publication describes the history of minimal intervention dentistry (MID) for managing dental caries and presents evidence for various carious lesion detection devices, for preventive measures, for restorative and non‐restorative therapies as well as for repairing rather than replacing defective restorations. It is a follow‐up to the FDI World Dental Federation publication on MID, of 2000. The dental profession currently is faced with an enormous task of how to manage the high burden of consequences of the caries process amongst the world population. If it is to manage carious lesion development and its progression, it should move away from the ‘surgical’ care approach and fully embrace the MID approach. The chance for MID to be successful is thought to be increased tremendously if dental caries is not considered an infectious but instead a behavioural disease with a bacterial component. Controlling the two main carious lesion development related behaviours, i.e. intake and frequency of fermentable sugars, to not more than five times daily and removing/disturbing dental plaque from all tooth surfaces using an effective fluoridated toothpaste twice daily, are the ingredients for reducing the burden of dental caries in many communities in the world. FDI's policy of reducing the need for restorative therapy by placing an even greater emphasis on caries prevention than is currently done, is therefore, worth pursuing.     

Systemic and local expression of perforin in lymphocyte subsets in acute and chronic rheumatoid arthritis

OBJECTIVE: To investigate the role of the cytolytic action mediated by perforin in the course of rheumatoid arthritis (RA), we studied the immunophenotypic characteristics of lymphocytes containing perforin in peripheral blood (systemic level), in synovial fluid (SF), and in the synovial membrane (local level) in patients during the acute or chronic phase of RA. Cells from patients with osteoarthritis were used as controls. METHODS: Flow cytometry was used for simultaneous detection of intracellular (perforin) and cell surface antigens. Mean fluorescence intensity (MFI) was a measure of the mean perforin content per cell. Immunocytochemical staining was used to visualize perforin in the cytoplasmic compartment of cells. RESULTS: In acute RA highly significant changes in perforin expression were found in all compartments (peripheral blood, SF, and synovial membrane): (1) increase of percentage of total perforin positive cells; (2) increase of both subsets of cytolytic cells, T (CD8+P+) and NK (CD56+P+) cells; (3) increase in the frequency of perforin positive cells in CD8+ and CD56+ cell populations; and (4) the highest content of perforin/cell (MFI values) in all compartments, except in the synovial membrane. CONCLUSION: Perforin positive cells may participate in the acute phase of RA by maintaining and perpetuating inflammation and contributing to tissue destruction.